Cryptosporidium parvum

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This page is about microbiologic aspects of the organism(s).  For clinical aspects of the disease, see Cryptosporidiosis.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];

Cryptosporidium parvum
Immunofluorescence image of C. parvum oocysts.
Immunofluorescence image of C. parvum oocysts.
Scientific classification
Kingdom: Protista
Phylum: Apicomplexa
Class: Conoidasida
Subclass: Coccidiasina
Order: Eucoccidiorida
Family: Cryptosporidiidae
Genus: Cryptosporidium
Species: C. parvum
Binomial name
Cryptosporidium parvum

Cryptosporidium parvum is one of several protozoal species that cause cryptosporidiosis, a parasitic disease of the mammalian intestinal tract.

Primary symptoms of C. parvum infection are acute, watery, and non-bloody diarrhea. C. parvum infection is of particular concern in immunocompromised patients, where diarrhea can reach 10–15L per day. Other symptoms may include anorexia, nausea/vomiting and abdominal pain. Extra-intestinal sites include the lung, liver and gall bladder where it causes respiratory cryptosporidosis, hepatitis and cholecystitis.[1][not in citation given]

Infection is caused by ingestion of sporulated oocysts transmitted by the faecal-oral route. In healthy human hosts, the median infective dose is 132 oocysts.[2] The general C. parvum life cycle is shared by other members of the genus. Invasion of the apical tip of ileal enterocytes by sporozoites and merozoites causes pathology seen in the disease.

Infection is generally self-limiting in immunocompetent people. In immunocompromised patients, such as those with AIDS or those undergoing immunosuppressive therapy, infection may not be self-limiting, leading to dehydration and, in severe cases, death.


Cryptosporidium parvum oocysts are very difficult to detect and therefore diagnose. The oocysts in fecal samples would indicate if the parasite is present in the body but they have a very small size and so detection is made very difficult. Doing a fecal ELISA method to detect the presence of the parasite would eliminate the difficulty due to the small size and many other methods are unable to distinguish between past and present infections; something serological ELISA would not allow to distinguish.[3]

C. parvum is considered to be the most important waterborne pathogen in developed countries. The protozoa also caused the largest waterborne-disease outbreak ever documented in the United States, making 403,000 people ill in Milwaukee, Wisconsin in 1993.[4] It is resistant to all practical levels of Water chlorination, surviving for 24hrs at 1000 mg/L free chlorine. It is an obligate intracellular pathogen.[5]


The most effective way to prevent the spread of Cryptosporidium parvum is to avoid the contact of feces that are contaminated. Avoiding this contact, especially with young children is important, as they are more likely to come into oral contact and have the parasite transferred into the body. These ideas of hygiene are the most effective way to combat this difficult to prevent parasite.[6]

Oocyst Stage

The Cryptosporidium parvum oocysts are incredibly durable and this can cause extended problems when attempting to control the spread of the parasite. The oocyst stage can tolerate a vast number of environmental pressures that allows it to be more likely to survive. The oocyst can tolerate temperatures as low as -22C and for long periods of time which means fecal contamination is possible even after going through those environmental extremes. The oocysts can also tolerate shifts in pH that are found in some water treatment process and careful attention to detail must be done to prevent the possibility of infection. The oocysts that are in fecal material are immediately infective and have the potential to find a new host if contamination occurs.[3][6]


The genome of C. parvum (sequenced in 2004[7]) have a relatively small size and simple organization of 9.1 Mb, which is composed of eight chromosomes ranging from 1.04 to 1.5 Mb. The genome is very compact, and is one of the few organisms without transposable elements. Unlike other apicomplexans, C. parvum has no genes in its plastids or mitochondria.[7]

Differential diagnosis

Cryptosporidium parvum infecton must be differentiated from other causes of viral, bacterial, and parasitic gastroentritis.

Organism Age predilection Travel History Incubation Size (cell) Incubation Time History and Symptoms Diarrhea type8 Food source Specific consideration
Fever N/V Cramping Abd Pain Small Bowel Large Bowel Inflammatory Non-inflammatory
Viral Rotavirus <2 y - <102 <48 h + + - + + - Mostly in day cares, most common in winter.
Norovirus Any age - 10 -103 24-48 h + + + + + - Most common cause of gastroenteritis, abdominal tenderness,
Adenovirus <2 y - 105 -106 8-10 d + + + + + - No seasonality
Astrovirus <5 y - 72-96 h + + + + + Seafood Mostly during winter
Bacterial Escherichia coli ETEC Any age + 108 -1010 24 h - + + + + - Causes travelers diarrhea, contains heat-labile toxins (LT) and heat-stable toxins (ST)
EPEC <1 y - 10 6-12 h - + + + + Raw beef and chicken -
EIEC Any ages - 10 24 h + + + + + Hamburger meat and unpasteurized milk Similar to shigellosis, can cause bloody diarrhea
EHEC Any ages - 10 3-4 d - + + + + Undercooked or raw hamburger (ground beef)  Known as E. coli O157:H7, can cause HUS/TTP.
EAEC Any ages + 1010 8-18 h - - + + + - May cause prolonged or persistent diarrhea in children
Salmonella sp. Any ages + 1 6 to 72 h + + + + + Meats, poultry, eggs, milk and dairy products, fish, shrimp, spices, yeast, coconut, sauces, freshly prepared salad. Can cause salmonellosis or typhoid fever.
Shigella sp. Any ages - 10 - 200 8-48 h + + + + + Raw foods, for example, lettuce, salads (potato, tuna, shrimp, macaroni, and chicken) Some strains produce enterotoxin and Shiga toxin similar to those produced by E. coli O157:H7
Campylobacter sp. <5 y, 15-29 y - 104 2-5 d + + + + + Undercooked poultry products, unpasteurized milk and cheeses made from unpasteurized milk, vegetables, seafood and contaminated water. May cause bacteremia, Guillain-Barré syndrome (GBS), hemolytic uremic syndrome (HUS) and recurrent colitis
Yersinia enterocolitica <10 y - 104 -106 1-11 d + + + + + Meats (pork, beef, lamb, etc.), oysters, fish, crabs, and raw milk. May cause reactive arthritis; glomerulonephritis; endocarditis; erythema nodosum.

can mimic appendicitis and mesenteric lymphadenitis.

Clostridium perfringens Any ages > 106 16 h - - + + + Meats (especially beef and poultry), meat-containing products (e.g., gravies and stews), and Mexican foods. Can survive high heat,
Vibrio cholerae Any ages - 106-1010 24-48 h - + + + + Seafoods, including molluscan shellfish (oysters, mussels, and clams), crab, lobster, shrimp, squid, and finfish. Hypotension, tachycardia, decreased skin turgor. Rice-water stools
Parasites Protozoa Giardia lamblia 2-5 y + 1 cyst 1-2 we - - + + + Contaminated water May cause malabsorption syndrome and severe weight loss
Entamoeba histolytica 4-11 y + <10 cysts 2-4 we - + + + + Contaminated water and raw foods May cause intestinal amebiasis and amebic liver abscess
Cryptosporidium parvum Any ages - 10-100 oocysts 7-10 d + + + + + Juices and milk May cause copious diarrhea and dehydration in patients with AIDS especially with 180 > CD4
Cyclospora cayetanensis Any ages + 10-100 oocysts 7-10 d - + + + + Fresh produce, such as raspberries, basil, and several varieties of lettuce. More common in rainy areas
Helminths Trichinella spp Any ages - Two viable larvae (male and female) 1-4 we - + + + + Undercooked meats More common in hunters or people who eat traditionally uncooked meats
Taenia spp Any ages - 1 larva or egg 2-4 m - + + + + Undercooked beef and pork Neurocysticercosis: Cysts located in the brain may be asymptomatic or seizures, increased intracranial pressure, headache.
Diphyllobothrium latum Any ages - 1 larva 15 d - - - + + Raw or undercooked fish. May cause vitamin B12 deficiency

8Small bowel diarrhea: watery, voluminous with less than 5 WBC/high power field

Large bowel diarrhea: Mucousy and/or bloody with less volume and more than 10 WBC/high power field
† It could be as high as 1000 based on patient's immunity system.

The table below summarizes the findings that differentiate inflammatory causes of chronic diarrhea[8][9][10][11][11]

Cause History Laboratory findings Diagnosis Treatment
Diverticulitis Abdominal CT scan with oral and intravenous (IV) contrast bowel rest, IV fluid resuscitation, and broad-spectrum antimicrobial therapy which covers anaerobic bacteria and gram-negative rods
Ulcerative colitis Endoscopy Induction of remission with mesalamine and corticosteroids followed by the administration of sulfasalazine and 6-Mercaptopurine depending on the severity of the disease.
Entamoeba histolytica cysts shed with the stool detects ameba DNA in feces Amebic dysentery

Luminal amebicides for E. histolytica in the colon:

For amebic liver abscess:


Supportive therapy such as IV fluids is the primary for C. parvum infection. Paromomycin and Nitazoxanide may alleviate some of the diarrhoeal symptoms, however the latter is contraindicated for AIDS patients. Continuing antiretroviral drugs to boost the immune system may also control infection. Research into other potential drugs and therapeutics targets, as well as vaccine candidates, is ongoing. Spiramycin for immunosuppressed patients.

Important C. parvum proteins and drug targets

Lipid metabolism

C. parvum is incapable of de novo lipid synthesis, making its lipid trafficking machinery an important potential therapeutic target. C. parvum possesses multiple oxysterol-binding proteins (OSBPs), and oxysterol related proteins (OSRPs). Only OSBPs are capable of lipid binding, while both contain Pleckstrin homology domains, which function in cell signalling pathways.

Surface glycoproteins

C. parvum possesses numerous surface glycoproteins thought to play a role in pathogenesis. An immunodominant >900kDa protein, known as GP900, localizes to the apical end of sporozoites and in micronemes of merozoites. Its high molecular mass is most likely due to heavy post-translational glycosylation. Indeed, the structure of GP900 is similar to that of a family of glycoproteins known as mucins. GP900 is thought to mediate attachment and invasion to host cells. GP900 may also play a role in C. parvum’s resistance to proteolysis by the numerous proteases found in the mammalian gut.

In vitro, hyperimmune sera as well as antibodies directed at specific epitopes on the GP900 protein inhibit the invasion of C. parvum sporozoites into MDCK cell monolayers. Additionally, competitive inhibition using native GP900 or purified GP900 fragments reduces cell invasion.[12]

Further experiments have confirmed the importance of the mucin-like glycosylations. Lectins directed at GP900 carbohydrate moieties (alpha-N-galactosamine) were able to block adhesion and prevent C. parvum invasion.[13]

C. parvum glycoproteins have the characteristics of attractive vaccine candidates. Many are immunodominant, and antibodies against select domains block invasion of host cells.


  1. ”Cryptosporidiosis.” Laboratory Identification of Parasites of Public Health Concern. CDC. 5 Sept 2007. <>
  2. DuPont HL, Chappell CL, Sterling CR, Okhuysen PC, Rose JB, Jakubowski W (March 1995). "The infectivity of Cryptosporidium parvum in healthy volunteers". N. Engl. J. Med. 332 (13): 855–9. doi:10.1056/NEJM199503303321304. PMID 7870140.
  3. 3.0 3.1 DuPont et al "The Infectivivty of Cryptosporidium parvum in healthy Volunteers"
  4. ”Surveillance for Waterborne-Disease Outbreaks -- United States, 1993-1994” CDC. 1996. <>
  5. Deng, M.; Lancto, C. A.; Abrahamsen, M. S. (2004). "Cryptosporidium parvum regulation of human epithelial cell gene expression". International Journal for Parasitology. 34 (1): 73–82. doi:10.1016/j.ijpara.2003.10.001. PMID 14711592.
  6. 6.0 6.1 Robertson et al "Survival of Cryposporidium parvum oocysts under various environmental pressures"
  7. 7.0 7.1 Abrahamsen MS, Templeton TJ; et al. (2004). "Complete genome sequence of the apicomplexan, Cryptosporidium parvum". Science. 304 (5669): 441–5. doi:10.1126/science.1094786. PMID 15044751. Retrieved 2008-05-25.
  8. Konvolinka CW (1994). "Acute diverticulitis under age forty". Am J Surg. 167 (6): 562–5. PMID 8209928.
  9. Silverberg MS, Satsangi J, Ahmad T, Arnott ID, Bernstein CN, Brant SR; et al. (2005). "Toward an integrated clinical, molecular and serological classification of inflammatory bowel disease: report of a Working Party of the 2005 Montreal World Congress of Gastroenterology". Can J Gastroenterol. 19 Suppl A: 5A–36A. PMID 16151544.
  10. Satsangi J, Silverberg MS, Vermeire S, Colombel JF (2006). "The Montreal classification of inflammatory bowel disease: controversies, consensus, and implications". Gut. 55 (6): 749–53. doi:10.1136/gut.2005.082909. PMC 1856208. PMID 16698746.
  11. 11.0 11.1 Haque R, Huston CD, Hughes M, Houpt E, Petri WA (2003). "Amebiasis". N Engl J Med. 348 (16): 1565–73. doi:10.1056/NEJMra022710. PMID 12700377.
  12. Barnes DA, Bonnin A, Huang JX; et al. (October 1998). "A novel multi-domain mucin-like glycoprotein of Cryptosporidium parvum mediates invasion". Mol. Biochem. Parasitol. 96 (1–2): 93–110. doi:10.1016/S0166-6851(98)00119-4. PMID 9851610.
  13. Cevallos AM, Bhat N, Verdon R; et al. (September 2000). "Mediation of Cryptosporidium parvum Infection In Vitro by Mucin-Like Glycoproteins Defined by a Neutralizing Monoclonal Antibody". Infect. Immun. 68 (9): 5167–75. doi:10.1128/IAI.68.9.5167-5175.2000. PMC 101770. PMID 10948140.